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[PMID]:28457516
[Au] Autor:Nakata M; Kasuda S; Yuui K; Kudo R; Hatake K
[Ad] Endereço:Department of Legal Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan. Electronic address: dc112064@naramed-u.ac.jp.
[Ti] Título:Relevance of hemolysis-induced tissue factor expression on monocytes in soft clot formation in alcohol-containing blood.
[So] Source:Leg Med (Tokyo);25:83-88, 2017 Mar.
[Is] ISSN:1873-4162
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The fluidity of cadaveric blood is an important characteristic in the post-mortem examination of cases of asphyxial death. Although it is empirically known that soft blood clots are present in cadaveric blood containing alcohol, the relationship between such clots and blood alcohol is unclear. We addressed this issue through in vitro studies using blood collected from healthy volunteers. Assessment of global hemostasis by rotational thromboelastometry revealed that ethanol treatment enhanced the procoagulant activity of whole blood. However, ethanol inhibited epinephrine-induced platelet aggregation, whereas plasma levels of von Willebrand factor and the activity of coagulation factors VIII and IX were unaffected. In contrast, tissue factor (TF) activity was higher in plasma obtained from ethanol-treated whole blood than that in plasma from untreated blood. Ethanol induced hemolysis of red blood cells, and the consequent hemoglobin (Hb) release promoted de novo synthesis of TF in isolated monocytes, as determined by real-time reverse transcription PCR, western blotting, and flow cytometry. However, ethanol itself did not induce TF expression in monocytes. Given that TF activates the extrinsic coagulation pathway and amplifies hemostatic reactions, Hb-induced TF expression in monocytes might contribute to soft blood clot formation.
[Mh] Termos MeSH primário: Coagulação Sanguínea/efeitos dos fármacos
Etanol/sangue
Hemólise
Monócitos/efeitos dos fármacos
Tromboplastina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Autopsia
Cadáver
Citometria de Fluxo
Medicina Legal
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3K9958V90M (Ethanol); 9035-58-9 (Thromboplastin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28957360
[Au] Autor:Matus V; Valenzuela JG; Hidalgo P; Pozo LM; Panes O; Wozniak A; Mezzano D; Pereira J; Sáez CG
[Ad] Endereço:Department of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
[Ti] Título:Human platelet interaction with E. coli O111 promotes tissue-factor-dependent procoagulant activity, involving Toll like receptor 4.
[So] Source:PLoS One;12(9):e0185431, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelets have a major role in clotting activation and contribute to the innate immune response during systemic infections. Human platelets contain tissue factor (TF) and express functional Toll-like receptor 4 (TLR4). However, the role of TLR4 in triggering the procoagulant properties of platelets, upon challenge with bacteria, is yet unknown. Our hypothesis is that E. coli O111-TLR4 interaction activates platelets and elicits their procoagulant activity. We demonstrated that the strain, but not ultrapure LPS, increased surface P-selectin expression, platelet dependent TF procoagulant activity (TF-PCA) and prompted a faster thrombin generation (TG). Blockade of TLR4 resulted in decreased platelet activation, TF-PCA and TG, revealing the participation of this immune receptor on the procoagulant response of platelets. Our results provide a novel mechanism by which individuals with bacterial infections would have an increased incidence of blood clots. Furthermore, the identification of platelet TF and TLR4 as regulators of the effect of E. coli O111 might represent a novel therapeutic target to reduce the devastating consequences of the hemostatic disorder during sepsis.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Plaquetas/metabolismo
Plaquetas/microbiologia
Escherichia coli/metabolismo
Tromboplastina/metabolismo
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Anticorpos Monoclonais/farmacologia
Coagulação Sanguínea/efeitos dos fármacos
Plaquetas/efeitos dos fármacos
Escherichia coli/efeitos dos fármacos
Seres Humanos
Lipoproteínas/farmacologia
Meia-Idade
Selectina-P/metabolismo
Ativação Plaquetária/efeitos dos fármacos
Plasma Rico em Plaquetas/metabolismo
Trombina/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Lipoproteins); 0 (P-Selectin); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 4); 0 (lipoprotein-associated coagulation inhibitor); 9035-58-9 (Thromboplastin); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185431


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[PMID]:28912365
[Au] Autor:Raffield LM; Zakai NA; Duan Q; Laurie C; Smith JD; Irvin MR; Doyle MF; Naik RP; Song C; Manichaikul AW; Liu Y; Durda P; Rotter JI; Jenny NS; Rich SS; Wilson JG; Johnson AD; Correa A; Li Y; Nickerson DA; Rice K; Lange EM; Cushman M; Lange LA; Reiner AP; NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, Hematology & Hemostasis TOPMed Working Group*
[Ad] Endereço:From the Department of Genetics (L.M.R., Q.D., Y. Li), Department of Biostatistics (Y. Li), and Department of Computer Science (Y. Li), University of North Carolina, Chapel Hill; Department of Pathology & Laboratory Medicine (N.A.Z., M.F.D., P.D., N.S.J., M.C.), and Department of Medicine (N.A.Z
[Ti] Título:D-Dimer in African Americans: Whole Genome Sequence Analysis and Relationship to Cardiovascular Disease Risk in the Jackson Heart Study.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2220-2227, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Plasma levels of the fibrinogen degradation product D-dimer are higher among African Americans (AAs) compared with those of European ancestry and higher among women compared with men. Among AAs, little is known of the genetic architecture of D-dimer or the relationship of D-dimer to incident cardiovascular disease. APPROACH AND RESULTS: We measured baseline D-dimer in 4163 AAs aged 21 to 93 years from the prospective JHS (Jackson Heart Study) cohort and assessed association with incident cardiovascular disease events. In participants with whole genome sequencing data (n=2980), we evaluated common and rare genetic variants for association with D-dimer. Each standard deviation higher baseline D-dimer was associated with a 20% to 30% increased hazard for incident coronary heart disease, stroke, and all-cause mortality. Genetic variation near was associated with higher D-dimer (rs2022030, ß=0.284, =3.24×10 ). The rs2022030 effect size was nearly 3× larger among women (ß=0.373, =9.06×10 ) than among men (ß=0.135, =0.06; interaction =0.009). The sex by rs2022030 interaction was replicated in an independent sample of 10 808 multiethnic men and women ( interaction =0.001). Finally, the African ancestral sickle cell variant ( rs334) was significantly associated with higher D-dimer in JHS (ß=0.507, =1.41×10 ), and this association was successfully replicated in 1933 AAs ( =2.3×10 ). CONCLUSIONS: These results highlight D-dimer as an important predictor of cardiovascular disease risk in AAs and suggest that sex-specific and African ancestral genetic effects of the and loci contribute to the higher levels of D-dimer among women and AAs.
[Mh] Termos MeSH primário: Afroamericanos/genética
Doenças Cardiovasculares/genética
Produtos de Degradação da Fibrina e do Fibrinogênio/análise
Hemoglobinas Anormais/genética
Traço Falciforme/genética
Tromboplastina/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Doenças Cardiovasculares/sangue
Doenças Cardiovasculares/etnologia
Doenças Cardiovasculares/mortalidade
Feminino
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Incidência
Masculino
Meia-Idade
Epidemiologia Molecular
Fenótipo
Prognóstico
Estudos Prospectivos
Medição de Risco
Fatores de Risco
Fatores Sexuais
Traço Falciforme/sangue
Traço Falciforme/etnologia
Traço Falciforme/mortalidade
Fatores de Tempo
Estados Unidos/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fibrin Fibrinogen Degradation Products); 0 (Hemoglobins, Abnormal); 0 (fibrin fragment D); 9035-58-9 (Thromboplastin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.310073


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[PMID]:28910348
[Au] Autor:Hellum M; Franco-Lie I; Øvstebø R; Hauge T; Henriksson CE
[Ad] Endereço:Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
[Ti] Título:The effect of corn trypsin inhibitor, anti-tissue factor pathway inhibitor antibodies and phospholipids on microvesicle-associated thrombin generation in patients with pancreatic cancer and healthy controls.
[So] Source:PLoS One;12(9):e0184579, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Circulating microvesicles (MVs) are suggested to be important contributors to cancer-associated thrombosis due to the presence of surface-bound procoagulant molecules like tissue factor (TF) and phosphatidylserine (PS). Pancreatic cancer is considered to be one of the most prothrombotic malignancies. The aim of this study was to describe the impact of analytical variables on MV-associated thrombin generation in patients with pancreatic cancer and in healthy controls. MVs were isolated from citrated plasma and added to pooled normal plasma (PNP). Thrombin generation was measured by the calibrated automated thrombogram. The impact of corn trypsin inhibitor (CTI), anti-tissue factor pathway inhibitor (TFPI) antibodies and phospholipids was described. Antibodies against TF were used to assess TF-dependency, and MV-bound PS activity was measured with the Zymuphen MP-activity kit. MVs from the pancreatic cancer patients displayed higher thrombin generation and higher PS-activity than MVs from the healthy control group, while TF-dependency was observed in only 1 out of 13 patient samples. Adequate thrombin generation-curves were only achieved when CTI was omitted and anti-TFPI antibodies were added to PNP prepared in low contact-activating tubes. Addition of phospholipids reduced the significant differences between the two groups, and should be omitted. This modified thrombin generation assay could be useful for measurement of procoagulant circulating MVs, allowing the contribution from MVs affecting both the intrinsic and the extrinsic pathway to be measured.
[Mh] Termos MeSH primário: Anticorpos/farmacologia
Micropartículas Derivadas de Células/metabolismo
Neoplasias Pancreáticas/metabolismo
Fosfolipídeos/farmacologia
Proteínas de Plantas/farmacologia
Trombina/metabolismo
[Mh] Termos MeSH secundário: Idoso
Micropartículas Derivadas de Células/efeitos dos fármacos
Feminino
Voluntários Saudáveis
Seres Humanos
Lipoproteínas/imunologia
Masculino
Meia-Idade
Neoplasias Pancreáticas/complicações
Fosfatidilserinas/metabolismo
Tromboplastina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Lipoproteins); 0 (Phosphatidylserines); 0 (Phospholipids); 0 (Plant Proteins); 0 (lipoprotein-associated coagulation inhibitor); 0 (trypsin inhibitor, Zea mays); 9035-58-9 (Thromboplastin); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184579


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[PMID]:28749986
[Au] Autor:Barska K; Kwiatkowska W; Knysz B; Arczynska K; Karczewski M; Witkiewicz W
[Ad] Endereço:Wrovasc-Integrated Cardiovascular Centre, Regional Specialist Hospital, Research and Development Center in Wroclaw, Wroclaw, Poland.
[Ti] Título:The role of the tissue factor and its inhibitor in the development of subclinical atherosclerosis in people living with HIV.
[So] Source:PLoS One;12(7):e0181533, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: HIV infection is associated with an increased risk of cardiovascular disease in connection with atherosclerosis and thromboembolic complications. The pathogenesis of atherosclerosis is still unclear in this group of patients. Studies on pathogenesis of atherosclerosis in the general population emphasize the role of the extrinsic pathway of blood coagulation, particularly the tissue factor (TF) and tissue factor pathway inhibitor (TFPI). The effect of persistent activation of the immune system on enhanced expression of TF on the surface of monocytes in subjects infected with HIV is known to be correlated with the level of HIV RNA in blood serum. STUDY AIM: The aim of this study was to evaluate the concentration of TF and its inhibitor TFPI in blood plasma, the impact of traditional and non-traditional cardiovascular risk factors on their concentration and the impact of both markers of haemostasis on the severity of subclinical atherosclerosis as assessed by the intima-media measurement of the carotid artery in HIV infected patients. MATERIALS: The study included 121 HIV-infected people with known clinical, immunological and virological status. The control group consisted of 42 healthy individuals, selected in terms of age and sex. RESULTS AND CONCLUSIONS: Higher concentrations of TF occurred in HIV-infected patients with a low current plasma HIV RNA level, nadir CD4+ T-cell count and longer duration of cumulative antiretroviral treatment. In multivariate analysis, it was the length of cumulative NRTI treatment that impacted on the concentration of TF. The determinants of cardiovascular disease (CVD) risk factors and inflammatory markers did not show any effect on the concentrations of TF. The TFPI level in HIV-infected patients was significantly higher than in the control group and was negatively correlated with the current level of HIV RNA and nadir CD4+ T-cell count, being higher in patients subjected to antiretroviral treatment. It was shown that the higher the cardiovascular risk and the higher the levels of total cholesterol, low-density lipoprotein cholesterol (LDL) and non-high-density lipoprotein cholesterol (non-HDL), the higher the concentrations of TFPI observed. The levels of TF and TFPI were positively correlated with carotid intima media thickness (cIMT); in the multivariate analysis, TF, non-HDL cholesterol and lifetime smoking (pack-years) independently affected the growth of cIMT. A similar effect on cIMT was demonstrated by TFPI.
[Mh] Termos MeSH primário: Aterosclerose/complicações
Infecções por HIV/sangue
Infecções por HIV/complicações
Lipoproteínas/sangue
Tromboplastina/metabolismo
[Mh] Termos MeSH secundário: Adulto
Aterosclerose/sangue
Biomarcadores/metabolismo
Espessura Intima-Media Carotídea
Estudos de Casos e Controles
Feminino
HIV/fisiologia
Seres Humanos
Mediadores da Inflamação/metabolismo
Modelos Lineares
Masculino
Meia-Idade
Análise Multivariada
RNA Viral/sangue
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Inflammation Mediators); 0 (Lipoproteins); 0 (RNA, Viral); 0 (lipoprotein-associated coagulation inhibitor); 9035-58-9 (Thromboplastin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181533


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[PMID]:28729433
[Au] Autor:Kamikubo Y; Mendolicchio GL; Zampolli A; Marchese P; Rothmeier AS; Orje JN; Gale AJ; Krishnaswamy S; Gruber A; Østergaard H; Petersen LC; Ruf W; Ruggeri ZM
[Ad] Endereço:Department of Molecular Medicine and.
[Ti] Título:Selective factor VIII activation by the tissue factor-factor VIIa-factor Xa complex.
[So] Source:Blood;130(14):1661-1670, 2017 Oct 05.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Safe and effective antithrombotic therapy requires understanding of mechanisms that contribute to pathological thrombosis but have a lesser impact on hemostasis. We found that the extrinsic tissue factor (TF) coagulation initiation complex can selectively activate the antihemophilic cofactor, FVIII, triggering the hemostatic intrinsic coagulation pathway independently of thrombin feedback loops. In a mouse model with a relatively mild thrombogenic lesion, TF-dependent FVIII activation sets the threshold for thrombus formation through contact phase-generated FIXa. In vitro, FXa stably associated with TF-FVIIa activates FVIII, but not FV. Moreover, nascent FXa product of TF-FVIIa can transiently escape the slow kinetics of Kunitz-type inhibition by TF pathway inhibitor and preferentially activates FVIII over FV. Thus, TF synergistically primes FIXa-dependent thrombin generation independently of cofactor activation by thrombin. Accordingly, FVIIa mutants deficient in direct TF-dependent thrombin generation, but preserving FVIIIa generation by nascent FXa, can support intrinsic pathway coagulation. In ex vivo flowing blood, a TF-FVIIa mutant complex with impaired free FXa generation but activating both FVIII and FIX supports efficient FVIII-dependent thrombus formation. Thus, a previously unrecognized TF-initiated pathway directly yielding FVIIIa-FIXa intrinsic tenase complex may be prohemostatic before further coagulation amplification by thrombin-dependent feedback loops enhances the risk of thrombosis.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Fator VIII/metabolismo
Fator VIIa/metabolismo
Fator Xa/metabolismo
Tromboplastina/metabolismo
[Mh] Termos MeSH secundário: Fator VIIIa/metabolismo
Seres Humanos
Trombina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
72175-66-7 (Factor VIIIa); 9001-27-8 (Factor VIII); 9035-58-9 (Thromboplastin); EC 3.4.21.21 (Factor VIIa); EC 3.4.21.5 (Thrombin); EC 3.4.21.6 (Factor Xa)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-02-767079


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[PMID]:28724635
[Au] Autor:Kotla S; Singh NK; Kirchhofer D; Rao GN
[Ad] Endereço:From the Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163 and.
[Ti] Título:Heterodimers of the transcriptional factors NFATc3 and FosB mediate tissue factor expression for 15( )-hydroxyeicosatetraenoic acid-induced monocyte trafficking.
[So] Source:J Biol Chem;292(36):14885-14901, 2017 Sep 08.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue factor (TF) is expressed in vascular and nonvascular tissues and functions in several pathways, including embryonic development, inflammation, and cell migration. Many risk factors for atherosclerosis, including hypertension, diabetes, obesity, and smoking, increase TF expression. To better understand the TF-related mechanisms in atherosclerosis, here we investigated the role of 12/15-lipoxygenase (12/15-LOX) in TF expression. 15( )-hydroxyeicosatetraenoic acid (15( )-HETE), the major product of human 15-LOXs 1 and 2, induced TF expression and activity in a time-dependent manner in the human monocytic cell line THP1. Moreover, TF suppression with neutralizing antibodies blocked 15( )-HETE-induced monocyte migration. We also found that NADPH- and xanthine oxidase-dependent reactive oxygen species (ROS) production, calcium/calmodulin-dependent protein kinase IV (CaMKIV) activation, and interactions between nuclear factor of activated T cells 3 (NFATc3) and FosB proto-oncogene, AP-1 transcription factor subunit (FosB) are involved in 15( )-HETE-induced TF expression. Interestingly, NFATc3 first induced the expression of its interaction partner FosB before forming the heterodimeric NFATc3-FosB transcription factor complex, which bound the proximal AP-1 site in the TF gene promoter and activated TF expression. We also observed that macrophages from 12/15-LOX mice exhibit diminished migratory response to monocyte chemotactic protein 1 (MCP-1) and lipopolysaccharide compared with WT mouse macrophages. Similarly, compared with WT macrophages, monocytes from 12/15-LOX mice displayed diminished trafficking, which was rescued by prior treatment with 12( )-HETE, in a peritonitis model. These observations indicate that 15( )-HETE-induced monocyte/macrophage migration and trafficking require ROS-mediated CaMKIV activation leading to formation of NFATc3 and FosB heterodimer, which binds and activates the TF promoter.
[Mh] Termos MeSH primário: Araquidonato 12-Lipoxigenase/metabolismo
Araquidonato 15-Lipoxigenase/metabolismo
Movimento Celular/efeitos dos fármacos
Ácidos Hidroxieicosatetraenoicos/farmacologia
Monócitos/efeitos dos fármacos
Fatores de Transcrição NFATC/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Tromboplastina/genética
[Mh] Termos MeSH secundário: Animais
Araquidonato 12-Lipoxigenase/deficiência
Araquidonato 12-Lipoxigenase/genética
Araquidonato 15-Lipoxigenase/deficiência
Araquidonato 15-Lipoxigenase/genética
Células Cultivadas
Seres Humanos
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monócitos/citologia
Monócitos/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Tromboplastina/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (12-15-lipoxygenase); 0 (FOSB protein, human); 0 (Hydroxyeicosatetraenoic Acids); 0 (NFATC Transcription Factors); 0 (NFATC3 protein, human); 0 (Proto-Oncogene Proteins c-fos); 0 (Reactive Oxygen Species); 9035-58-9 (Thromboplastin); EC 1.13.11.31 (Arachidonate 12-Lipoxygenase); EC 1.13.11.33 (Arachidonate 15-Lipoxygenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.804344


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[PMID]:28699284
[Au] Autor:Solovey A; Somani A; Belcher JD; Milbauer L; Vincent L; Pawlinski R; Nath KA; Kelm RJ; Mackman N; O'Sullivan MG; Gupta K; Vercellotti GM; Hebbel RP
[Ad] Endereço:Division of Hematology-Oncology-Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota.
[Ti] Título:A monocyte-TNF-endothelial activation axis in sickle transgenic mice: Therapeutic benefit from TNF blockade.
[So] Source:Am J Hematol;92(11):1119-1130, 2017 Nov.
[Is] ISSN:1096-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elaboration of tumor necrosis factor (TNF) is a very early event in development of ischemia/reperfusion injury pathophysiology. Therefore, TNF may be a prominent mediator of endothelial cell and vascular wall dysfunction in sickle cell anemia, a hypothesis we addressed using NY1DD, S+S , and SS-BERK sickle transgenic mice. Transfusion experiments revealed participation of abnormally activated blood monocytes exerting an endothelial activating effect, dependent upon Egr-1 in both vessel wall and blood cells, and upon NFκB(p50) in a blood cell only. Involvement of TNF was identified by beneficial impact from TNF blockers, etanercept and infliximab, with less benefit from an IL-1 blocker, anakinra. In therapeutic studies, etanercept ameliorated multiple disturbances of the murine sickle condition: monocyte activation, blood biomarkers of inflammation, low platelet count and Hb, vascular stasis triggered by hypoxia/reoxygenation (but not if triggered by hemin infusion), tissue production of neuro-inflammatory mediators, endothelial activation (monitored by tissue factor and VCAM-1 expression), histopathologic liver injury, and three surrogate markers of pulmonary hypertension (perivascular inflammatory aggregates, arteriolar muscularization, and right ventricular mean systolic pressure). In aggregate, these studies identify a prominent-and possibly dominant-role for an abnormal monocyte-TNF-endothelial activation axis in the sickle context. Its presence, plus the many benefits of etanercept observed here, argue that pilot testing of TNF blockade should be considered for human sickle cell anemia, a challenging but achievable translational research goal.
[Mh] Termos MeSH primário: Anemia Falciforme/metabolismo
Células Endoteliais/metabolismo
Monócitos/metabolismo
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Anemia Falciforme/diagnóstico
Anemia Falciforme/tratamento farmacológico
Anemia Falciforme/genética
Animais
Anticorpos Monoclonais/farmacologia
Biomarcadores
Transplante de Medula Óssea
Agregação Celular/genética
Agregação Celular/imunologia
Modelos Animais de Doenças
Proteína 1 de Resposta de Crescimento Precoce/genética
Proteína 1 de Resposta de Crescimento Precoce/metabolismo
Endotélio Vascular/metabolismo
Etanercepte/farmacologia
Etanercepte/uso terapêutico
Testes de Função Cardíaca
Seres Humanos
Mediadores da Inflamação
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/imunologia
Leucócitos Mononucleares/metabolismo
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Terapia de Alvo Molecular
Monócitos/efeitos dos fármacos
Monócitos/imunologia
NF-kappa B/deficiência
NF-kappa B/genética
Fenótipo
Inibidores de Proteínas Quinases/farmacologia
Transdução de Sinais/efeitos dos fármacos
Tromboplastina/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Biomarkers); 0 (Early Growth Response Protein 1); 0 (Egr1 protein, mouse); 0 (Inflammation Mediators); 0 (NF-kappa B); 0 (Protein Kinase Inhibitors); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 9035-58-9 (Thromboplastin); OP401G7OJC (Etanercept)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1002/ajh.24856


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[PMID]:28686711
[Au] Autor:Zhalyalov AS; Panteleev MA; Gracheva MA; Ataullakhanov FI; Shibeko AM
[Ad] Endereço:Center for Theoretical Problems of Physicochemical Pharmacology RAS, Moscow, Russia.
[Ti] Título:Co-ordinated spatial propagation of blood plasma clotting and fibrinolytic fronts.
[So] Source:PLoS One;12(7):e0180668, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fibrinolysis is a cascade of proteolytic reactions occurring in blood and soft tissues, which functions to disintegrate fibrin clots when they are no more needed. In order to elucidate its regulation in space and time, fibrinolysis was investigated using an in vitro reaction-diffusion experimental model of blood clot formation and dissolution. Clotting was activated by a surface with immobilized tissue factor in a thin layer of recalcified blood plasma supplemented with tissue plasminogen activator (TPA), urokinase plasminogen activator or streptokinase. Formation and dissolution of fibrin clot was monitored by videomicroscopy. Computer systems biology model of clot formation and lysis was developed for data analysis and experimental planning. Fibrin clot front propagated in space from tissue factor, followed by a front of clot dissolution propagating from the same source. Velocity of lysis front propagation linearly depended on the velocity clotting front propagation (correlation r2 = 0.91). Computer model revealed that fibrin formation was indeed the rate-limiting step in the fibrinolysis front propagation. The phenomenon of two fronts which switched the state of blood plasma from liquid to solid and then back to liquid did not depend on the fibrinolysis activator. Interestingly, TPA at high concentrations began to increase lysis onset time and to decrease lysis propagation velocity, presumably due to plasminogen depletion. Spatially non-uniform lysis occurred simultaneously with clot formation and detached the clot from the procoagulant surface. These patterns of spatial fibrinolysis provide insights into its regulation and might explain clinical phenomena associated with thrombolytic therapy.
[Mh] Termos MeSH primário: Coagulação Sanguínea/genética
Fibrinólise/genética
Terapia Trombolítica
[Mh] Termos MeSH secundário: Simulação por Computador
Fibrina/genética
Fibrina/metabolismo
Seres Humanos
Plasminogênio/metabolismo
Estreptoquinase/sangue
Tromboplastina/metabolismo
Ativador de Plasminogênio Tecidual/sangue
Ativador de Plasminogênio Tipo Uroquinase/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9001-31-4 (Fibrin); 9001-91-6 (Plasminogen); 9035-58-9 (Thromboplastin); EC 3.4.- (Streptokinase); EC 3.4.21.68 (PLAT protein, human); EC 3.4.21.68 (Tissue Plasminogen Activator); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180668


  10 / 8681 MEDLINE  
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[PMID]:28671072
[Au] Autor:Conversy B; Blais MC; Dunn M; Gara-Boivin C; Del Castillo JRE
[Ad] Endereço:Department of Clinical Sciences, Faculté de Médecine Métérinaire, Université de Montréal, C.P. 5000, Saint-Hyacinthe, Québec J2S 7C6, Canada. Electronic address: berenice.conversy@umontreal.ca.
[Ti] Título:Anticoagulant activity of oral rivaroxaban in healthy dogs.
[So] Source:Vet J;223:5-11, 2017 May.
[Is] ISSN:1532-2971
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rivaroxaban is an oral, direct factor Xa inhibitor used in human thrombotic disorders. In view of the in vitro concentration dependent anticoagulant effects of rivaroxaban in dogs, the time course of its anticoagulant effects was characterized in healthy dogs. Twenty-four healthy Beagles were randomized into three groups (n = 8 per group) and received orally either a placebo or 20 mg rivaroxaban once or twice at an 8 h interval. Fifteen blood samples were collected over a 30 h period, and blindly assayed for prothrombin time (PT), activated partial thromboplastin time (aPTT), tissue factor induced thrombin generation (TG) and anti-factor Xa activity. Thromboelastography (TEG) was evaluated at 0, 1, 4, 8 and 24 h. Peak/baseline anticoagulant effect ratios were analyzed with generalized linear models using ß distributions and times to return to baseline with survival analyses (α = 0.05). Peak/baseline anticoagulant effect ratios of PT, aPTT, anti-factor Xa activity, TG and R (TEG) differed significantly between placebo and both rivaroxaban groups (P <0.0001). The peak anticoagulant effect of rivaroxaban occurred 1.5 to 2 h after dosing. The median return to baseline occurred significantly sooner (P <0.01) with 20 mg rivaroxaban administered once (7.9-18.7 h) versus twice (17.5-26.8 h). The inter-individual variability differed amongst assays, but overall was moderate to large. No adverse effects were recorded. Twice oral administration of 2 mg/kg rivaroxaban at an 8 h interval maintained 24 h anticoagulant activity, but larger studies are needed to establish guidelines for the use of rivaroxaban in dogs.
[Mh] Termos MeSH primário: Anticoagulantes
Cães/sangue
Rivaroxabana/farmacologia
Rivaroxabana/farmacocinética
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/farmacocinética
Anticoagulantes/farmacologia
Disponibilidade Biológica
Testes de Coagulação Sanguínea/veterinária
Inibidores do Fator Xa/sangue
Feminino
Tempo de Tromboplastina Parcial
Placebos
Tempo de Protrombina
Rivaroxabana/administração & dosagem
Trombina/biossíntese
Tromboplastina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Factor Xa Inhibitors); 0 (Placebos); 9035-58-9 (Thromboplastin); 9NDF7JZ4M3 (Rivaroxaban); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE



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